ArticleLeukemia2017
HBZ-mediated shift of JunD from growth suppressor to tumor promoter in leukemic cells by inhibition of ribosomal protein S25 expression.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Review
- Multi-omics profiling reveals intrathymic triggers and novel biomarkers in thymoma-associated myasthenia gravis.Biomarker research · 2026Article
- Valproate reactivates HTLV-1 tax and reduces ABCB1/MDR1 expression in PBMCs derived from ATLL patients.Frontiers in oncology · 2026Article
- Article
- APIR: Aggregating Universal Proteomics Database Search Algorithms for Peptide Identification with FDR Control.Genomics, proteomics & bioinformatics · 2024Article
- Deep learning for detecting and elucidating human T-cell leukemia virus type 1 integration in the human genome.Patterns (New York, N.Y.) · 2023Article
- Exploring hTERT promoter methylation in cutaneous T-cell lymphomas.Molecular oncology · 2022Article
- Alternative RNA splicing in cancer: what about adult T-cell leukemia?Frontiers in immunology · 2022Review
- A newly identified interaction between nucleolar NPM1/B23 and the HTLV-I basic leucine zipper factor in HTLV-1 infected cells.Frontiers in microbiology · 2022Article
- Deep learning-based transcriptome model predicts survival of T-cell acute lymphoblastic leukemia.Frontiers in oncology · 2022Article
- HTLV-1 persistence and leukemogenesis: A game of hide-and-seek with the host immune system.Frontiers in immunology · 2022Review
- Article
- HTLV-1 bZIP factor: the key viral gene for pathogenesis.Retrovirology · 2020Review
- miR-204-5p Represses Bone Metastasis via Inactivating NF-κB Signaling in Prostate Cancer.Molecular therapy. Nucleic acids · 2019Article
- Silencers of HTLV-1 and HTLV-2: the pX-encoded latency-maintenance factors.Retrovirology · 2019Review
- The SUMO Pathway in Hematomalignancies and Their Response to Therapies.International journal of molecular sciences · 2019Review
- Collagen IV (COL4A1, COL4A2), a Component of the Viral Biofilm, Is Induced by the HTLV-1 Oncoprotein Tax and Impacts Virus Transmission.Frontiers in microbiology · 2019Article
- HTLV-1 Alters T Cells for Viral Persistence and Transmission.Frontiers in microbiology · 2018Review
- Hijacking of the AP-1 Signaling Pathway during Development of ATL.Frontiers in microbiology · 2017Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) basic-leucine zipper (bZIP) factor (HBZ) is a key player in proliferation and transformation of HTLV-1-infected cells, thus contributing to adult T-cell leukemia (ATL) development. HBZ deregulates gene expression within the host cell by interacting with several cellular partners. Through its C-terminal ZIP domain, HBZ is able to contact and activate JunD, a transcription factor of the AP-1 family. JunD mRNA is intronless but can generate two protein isoforms by alternative translation initiation: JunD full-length and Δ JunD, an N-terminal truncated form unresponsive to the tumor suppressor menin. Using various cell lines and primary T-lymphocytes, we show that after serum deprivation HBZ induces the expression of Δ JunD isoform. We demonstrate that, unlike JunD, Δ JunD induces proliferation and transformation of cells. To decipher the mechanisms for Δ JunD production, we looked into the translational machinery and observed that HBZ induces nuclear retention of RPS25 mRNA and loss of RPS25 protein expression, a component of the small ribosomal subunit. Therefore, HBZ bypasses translational control of JunD uORF and favors the expression of Δ JunD. In conclusion, we provide strong evidences that HBZ induces Δ JunD expression through alteration of the cellular translational machinery and that the truncated isoform Δ JunD has a central role in the oncogenic process leading to ATL.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.